Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 301, Issue 1-2, Pages 163-168Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.10.047
Keywords
Hydroxysteroid (17 beta) dehydrogenase 1; Transgenic mice; Masculinization
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Funding
- Hormos Medical Ltd.
- QuatRx Pharmaceuticals
- Turku Graduate School of Biomedical Sciences
- Finnish Cultural Foundation
- Finnish Union of Experts in Science
- MRC [MC_U127685844, MC_U127685841] Funding Source: UKRI
- Medical Research Council [MC_U127685841, MC_U127685844] Funding Source: researchfish
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When present in excess amounts during fetal life, androgens can impair female development by inducing masculinization. On way to modify fetal steroid concentration is by altering the expression of hydroxysteroid (17 beta) dehydrogenases (HSD17Bs). Human HSD17B1 converts weak estrogen estrone to estradiol, and with lower catalytic efficiency, weak androgen androstenedione to testosterone. We have recently shown that over-expression of human HSD17B1 in transgenic mice results in masculinized phenotype in female mice. In the present study, we further show that in addition to the Mullerian ducts, HSD17B1TG females have internal structures resembling Wolffian ducts, and enlarged Skene paraurethral gland, also called the female prostate. HSD17B1 expression has been found in fetal human ovary, thus, it is possible that HSD17B1 contributes to maintain the normal steroid hormone concentration during development. Thereby, abnormal increase in the fetal expression of HSD17B1 could contribute to the development of hormonal imbalances, and so result in female masculinization. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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